Since the early eighties at the institute of Physiology of University of Goettingen Gersing and Preusse started to investigate myocardial impedance during ischemia in animal experiments. It was found that ischemia induced alterations in morphology and metabolism could be detected very early by this method.

In a preliminary clinical study we have performed first impedance measurements in 19 human hearts during open heart procedures. All patients suffered from coronary heart disease (CHD). There were 12 men and 7 women. Mean age was 61.7 years (range 50 - 83 years). Six patients had 2-vessel-disease while the remaining 13 patients had 3-vessel-disease. During the operative procedure 2.8 grafts/pt (vein grafts and/or LIMA grafts) were performed. For myocardial protection intermittent aortic cross damping at mild systemic hypothermia at 28 °C with ventricular fibrillation was used. Ischemia periods lasted for about 12 min each. After having performed each “coronary” anastomosis the aortic clamp was removed and the heart was perfused aerobicly for 5 minutes. Myocardial impedance measurements were atraumaticly performed shortly before every aortic declamping and before aortic re-clamping. The probe was a flat disc with 4 parallel platin electrodes: by the outer ones the alternating current (0.1 - 1 MHz) was injected into the epicardial layer of the myocardium, while by the inner ones corresponding voltages were measured. Measuring periods lasted for about 5 seconds. During the first two cross clamping periods (= ischemia) real part Re (Z) increased to about 20 % at 1 KHz current. Phase angle (ϕ) at 100 KHz increased to 8 % respectively 17 % within the same periods.

During the corresponding aerobic reperfusion periods Re (Z) at 1 KHz almost returned to initial preischemic values while phase angle (ϕ) values went below the initial preischemic values. At the end of the third ischemic period Re only increases to 6 %, while phase angle did not show any change. During reperfusion period both parameters did not reach the initial preischemic values any longer.

Besides the two above mentioned parameters we have also calculated the extracellular space index (ESI) being the quotient of Re (Z) at high frequency (1MHz) to Re (Z) at low frequency (300 Hz). By this parameter we could demonstrate that during the first two periods of ischemia ESI decreased, while later on an intraischemic increase could be analyzed.

Interpretating our results we could ascertain that during the first two periods of ischemia an intracellular oedema was developing, that reversibly disappeared during the following reperfusion periods. The changing values of ESI indicate such pathophysiological alterations. Additionally the increase of intracellular space was indirectly indicated by the increase of Re (Z) at a high frequency. Constant Re (Z) at the end of the third ischemic period and the decrease of Re (Z) below initial values during aerobic reperfusion may be interpreted by two different hypotheses: Either an extracellular oedema was developing or the active and passive alterations of conductivities of myocardial membranes for electrolytes have occurred.

Our results demonstrate that by impedance spectroscopy structural and metabolic alterations of the myocardium during ischemia-reperfusion may be early detected. So this method may be useful for improvement of therapeutical strategies to minimize ischemia-reperfusion injuries.